IMMUNOLOCALIZATION OF RAT CARDIAC BETA-MHC PROTEIN EXPRESSION IN SYSTEMIC HYPERTENSION AND CALORIC RESTRICTION

Citation
Sj. Swoap et al., IMMUNOLOCALIZATION OF RAT CARDIAC BETA-MHC PROTEIN EXPRESSION IN SYSTEMIC HYPERTENSION AND CALORIC RESTRICTION, American journal of physiology. Cell physiology, 38(4), 1995, pp. 1034-1041
Citations number
30
Categorie Soggetti
Physiology
ISSN journal
03636143
Volume
38
Issue
4
Year of publication
1995
Pages
1034 - 1041
Database
ISI
SICI code
0363-6143(1995)38:4<1034:IORCBP>2.0.ZU;2-C
Abstract
Previous studies have shown that both systemic hypertension induced by abdominal aortic constriction (Abcon) and 50% caloric restriction (CR ) increase left ventricular (LV) beta-myosin heavy chain (MHC) protein expression in the rat. However, these two physiological states have d ifferent effects on hemodynamic load, and information regarding beta-M HC localization across the LV wall in these two models may provide ins ight into the process of adaptation to chronic stress among myocardial cells. Thus the goal of this study was to determine the pattern of be ta-MHC protein expression across the LV wall in Abcon and CR models us ing a beta-MHC-specific antibody. Adult female Sprague-Dawley rats (si milar to 225-250 g) were randomly assigned to one of three groups: 1) normal control (NC), 2) Abcon, and 3) CR. After a treatment period of 5 wk, Abcon LVs hypertrophied 52% relative to NC, accompanying the 42% increase in mean blood pressure. CR rats, however, had a normal LV we ight-to-body weight ratio. The relative content of LV beta-MHC protein expression, as assessed by native gel electrophoresis, increased from 3% in NC to 25 and 41% in Abcon and CR rats, respectively. Immunohist ochemical analysis of beta-MHC expression demonstrated that the increa se in beta-MHC protein in the Abcon group occurred primarily on the en docardial side of the LV. In contrast, the increase in beta-MHC protei n in the CR LV occurred equally across the entire LV wall. This sugges ts that CR has a global effect on MHC isoform expression in LV myocard ial cells. Thus the models of Abcon and CR affected different populati ons of myocardial cells, consistent with previous findings suggesting that these models upregulate beta-MHC expression via different pathway s.